Pectolinarin通过PI3K/AKT信号通路调节小胶质细胞极化促进脊髓损伤后功能恢复

IF 4.6 2区 医学 Q1 NEUROSCIENCES
Molecular Neurobiology Pub Date : 2025-07-01 Epub Date: 2025-02-27 DOI:10.1007/s12035-025-04793-w
Chenggui Wang, Jiawei Li, Chenyu Wu, Zhouwei Wu, Zhichen Jiang, Chenglong Hong, Juntao Ying, Fancheng Chen, Qi Yang, Hui Xu, Sunren Sheng, Yongzeng Feng
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引用次数: 0

摘要

脊髓损伤后,小胶质细胞极化在脊髓恢复和轴突再生中起着重要作用。在这项研究中,我们进行了mRNA微阵列来鉴定与不同小胶质细胞表型相关的基因。结果显示,小胶质细胞极化与PI3K/AKT信号通路之间存在相关性,PI3K/AKT信号通路是炎症反应的关键调节因子。此外,我们发现Pectolinarin (PTR)可以通过直接抑制PI3K/AKT信号通路,有效抑制脂多糖(LPS)诱导的小胶质细胞M1极化,促进其向M2表型过渡。在我们建立的脊髓损伤动物模型中,我们证实PTR治疗诱导小胶质细胞向M2表型极化,导致纤维瘢痕形成减少,髓鞘重建增强,轴突再生改善。综上所述,PTR靶向PI3K/AKT信号通路是脊髓损伤治疗的一个有希望的新方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pectolinarin Promotes Functional Recovery after Spinal Cord Injury by Regulating Microglia Polarization Through the PI3K/AKT Signaling Pathway.

After spinal cord injury (SCI), microglia polarization plays an important role in spinal cord recovery and axon regeneration. In this study, we conducted mRNA microarrays to identify genes associated with different microglial phenotypes. The results showed a correlation between microglial polarization and the PI3K/AKT signaling pathway, a key regulator of inflammatory responses. In addition, we found that Pectolinarin (PTR) could effectively inhibit lipopolysaccharide (LPS)-induced M1 polarization of microglia and facilitate their transition to the M2 phenotype by directly suppressing the PI3K/AKT signaling pathway. In our established animal model of SCI, it was confirmed that PTR treatment induced microglial polarization towards the M2 phenotype, resulting in reduced fibrous scar formation, enhanced myelin reconstitution, and improved axonal regeneration. In conclusion, targeting the PI3K/AKT signaling pathway with PTR presents a promising new direction for SCI treatment.

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来源期刊
Molecular Neurobiology
Molecular Neurobiology 医学-神经科学
CiteScore
9.00
自引率
2.00%
发文量
480
审稿时长
1 months
期刊介绍: Molecular Neurobiology is an exciting journal for neuroscientists needing to stay in close touch with progress at the forefront of molecular brain research today. It is an especially important periodical for graduate students and "postdocs," specifically designed to synthesize and critically assess research trends for all neuroscientists hoping to stay active at the cutting edge of this dramatically developing area. This journal has proven to be crucial in departmental libraries, serving as essential reading for every committed neuroscientist who is striving to keep abreast of all rapid developments in a forefront field. Most recent significant advances in experimental and clinical neuroscience have been occurring at the molecular level. Until now, there has been no journal devoted to looking closely at this fragmented literature in a critical, coherent fashion. Each submission is thoroughly analyzed by scientists and clinicians internationally renowned for their special competence in the areas treated.
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